[Analysis of morphological manifestations of the inflammatory reaction in wistar rat spinal cord in experimental model].

Morphological changes in the spinal cord of rats with different intensity of pathological symptoms were studied at the peak of the experimental encephalomyelitis development. Light-microscopical and immunohistochemical methods were used. Distribution of proliferating cell nuclear antigen (PCNA), astrocyte marker - glial fibrillar acidic protein (GFAP), and microglia and macrophage marker Iba-1, was studied.

[Disordered permeability of the hemato-encephalic barrier in the development of allergic processes of the nervous system].

A single intravenous injection of dimethyl sulfoxide disturbed permeability of the blood-brain barrier (BBB) and caused passage of rhodamin from the blood into the brain in guinea pigs. Brain microinjury, injection of Freund's complete adjuvant or dimethyl sulfoxide increased BBB permeability to brain antigens detected in the animals' blood as early as the first 24 hours after the procedure. Antibodies appeared in the serum and/or delayed type hypersensitivity cell reactions formed in some of the animals later.

[Immunomorphologic features of experimental allergic encephalomyelitis induced by the administration of tryptophan peptide].

Three patterns of EAE with different morbidity and mortality rates were induced in the guinea pigs inoculated with various doses of tryptophane peptide (TP) and complete Freund's adjuvant. TP-sensitized animals manifested the delayed type hypersensitivity (DTH) reactions to TP and circulating anti-TP and -BPF antibodies were not found, polypeptide fraction of myelin basic protein (BPF while a A correlation was revealed between the DTH-reactions and EAE development. Intracutaneous TP and BPF injections at the early period before the EAE onset resulted in reduction of morbidity rate from 90 to 50 per cent.

[A method of detecting demyelinated nerve tissue in experimental allergic encephalomyelitis].

A method of rapid pathomorphological diagnosis of demyelinization with a simultaneous detection of cell elements in the nervous tissue has been described. The method tested on the model of experimental allergic encephalomyelitis (EAE) is a modified method of Marchi with subsequent staining of histological sections with toluidine blue. Due to a shorter period of nervous tissue exposure to potassium bichromate and osmium acid solutions (from 6-8 weeks to 5 days) the cells preserve their ability to uptake the dye and the endurance of histological sections increases.

[Immunomorphological characteristics of experimental allergic encephalomyelitis induced by an encephalitogenic polypeptide].

Encephalitogenic, immunogenic properties of the polypeptide fraction of myelin basic protein (FBP) and CNS lesions have been examined in animals with experimental allergic encephalomyelitis (EAE). FBP was isolated from bovine spinal cord using column chromatography. Administration of 1.

[Dynamics of pathomorphologic changes in experimental allergic encephalomyelitis].

The new method of simultaneous identification of myelin degradation products and cellular elements in the demyelinated nervous tissue allowed one to determine some previously unknown regularities in the interaction of demyelination and inflammation processes during experimentally induced allergic encephalomyelitis. The most significant feature in the pathomorphology of this disease is shown to be the change in osmiophilia and the amount of myelin degradation products in the demyelination foci, with every stage of periaxonal changes corresponding to a certain type of cellular reactions. A close relation is revealed between the demyelination and inflammation processes determining the structure of demyelination foci at different stages of the disease.

[Neurologic manifestations and periaxonal demyelination in the central nervous system in different forms of experimental allergic encephalomyelitis].

Comparing the neurological manifestations of experimentally-induced allergic encephalomyelitis (EAE) with the topography of developing demyelinization in the central nervous system of guinea-pigs allowed the authors to identify three forms of the diseases, namely spinal, cerebral and mixed. The spinal form caused by myelin decay in the lumbosacral segments of the spinal cord was expressed in the form of pareses and paralyses affecting the hind paws and also pelvic disorders. In the cerebral form, demyelinization was localized in the brain and was most frequently attended by vestibular disturbances.

[Prevention of experimental allergic encephalomyelitis in guinea pigs by treatment with magnetophores].

Subcutaneous application of magnetophores with a field intensity of 210 ersted prevented the development of experimental allergic encephalomyelitis (EAE) in guinea-pigs. The magnetophores appeared efficacious both at the beginning of the induction period and in the second half of the latent period, i.e.

[Induction of experimental allergic encephalomyelitis with encephalitogenic myelin proteins from the spinal cord of a bull].

A homogenous base protein, exhibiting high encephalitogenic activity towards guinea pigs and rabbits, was isolated from bovine spinal cord using column chromatography. Administration of the preparation obtained together with Freund's adjuvant into the animals caused development of neurogic symptoms typical for experimental allergic encephalomyelitis as well as formation of demyelinization foci both in spinal cord and in brain of guinea pigs and rabbits.

[Isolation and analysis of encephalitogenic fractions of spinal cord proteins].

Main encephalitogenic protein was isolated from bovine medulla spinalis and separated into homogenous polypeptide fractions by gel filtration; some of these fractions had the high encephalitogenic activity. The main protein and its fractions, possessing the encephalitogenic activity, caused a development of cross-reacting antibodies and a sensitization to intracutaneous administration of encephalitogenic preparations in animals. Non-encephalitogenic main protein sensitized animals only to this protein and did not induce the formation of distinct amount of antibodies.

[Effect of antibodies to rat and human cerebral cortex and white matter on heterologous T- and B-cells].

A study was made of the cytotoxic and complement-fixation activity of the antisera to the cortex and white matter of the rat and human brain upon the mouse and rat thymus and bone marrow cells. The cytotoxicity test proved to be more sensitive and precise. Cytotoxins to rodent thymocytes were revealed on ly in the antisera against the human brain cortex; at the same time they were revealed both in the antisera against the cortex and against the white matter of the rat brain (much more was found in the former).

[Influence of antilymphocyte sera on the development of experimental allergic encephalomyelitis].

Experimental allergic encephalomyelitis (EAE) was induced in guinea pigs by sensitization of myelinomas of homologous or heterologous (rabbit) brain in the complete Freund's adjuvant. Antilymphocytic serum (ALS) obtained by immunization of rabbits with the lymphocytes of the lymph nodes of guinea pigs was injected subcutaneously for 3--6 days at the early periods before or after the sensitization. ALS produced a marked inhibitory action on the development of the neurological signs of EAE and of histological changes in the form of demyelinization and perivascular cell infiltration in the lumbo-sacral and cervical portions of the spinal cord.

[Presence of cross-reacting thymus and brain antigens in the cerebral cortex].

Rabbit antisera against antigens of mouse, rabbit, guinea pig and human whole brain cross-reacted in the cytotoxic test with the lymphocytes of the thymus, lymph nodes and the spleen of these animal species. Mouse thymocytes were most sensitive to the antibrain sera (cytotoxic index -- 63--100 per cent); cells from other mouse lymphoid organs and lymphocytes of rabbit, guinea pig and man were more resistant. Bone marrow lymphocytes were not damaged by any of these sera.